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This study aims to evaluate the synergistic effects of hesperadin and chidamide on T-cell acute lymphoblastic leukemia (T-ALL).

December 8, 2025Blood

Hesperadin, an aurora B kinase inhibitor, synergizes with chidamide to suppress T-cell acute lymphoblastic leukemia by targeting c-MYC

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Combination of hesperadin and chidamide reduces tumor growth in T-ALL, indicating effective MYC modulation.

This study aims to evaluate the synergistic effects of hesperadin and chidamide on T-cell acute lymphoblastic leukemia (T-ALL).
Assessed the cytotoxicity of hesperadin and chidamide in T-ALL cell lines using CCK-8 assays.
Evaluated in vivo efficacy with T-ALL xenograft models.
Calculated IC₅₀ values with GraphPad Prism and analyzed drug synergy with CompuSyn.
Conducted flow cytometry and Western blot to assess apoptosis, cell cycle dynamics, and signaling pathways.
Studied MYC protein turnover using cycloheximide pulse-chase assays.
Hesperadin demonstrated potent cytotoxicity in T-ALL cells with IC₅₀ values between 0.14 and 0.4 µM.
Induced apoptosis through upregulation of Bax and downregulation of BCL2/MCL1.
Caused G₂/M cell cycle arrest with decreased CDK1 and Cyclin B levels.
Promoted MYC protein degradation without affecting MYC mRNA levels.
The combination with chidamide significantly inhibited cell proliferation and suppressed tumor growth in vivo.

Zhaoxing Wu (2025) studied this question.

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